Harding R K, Morris G P
Gastroenterology. 1977 May;72(5 Pt 1):857-63.
The gastric mucosa is characterized by high rates of surface epithelial cell (SEC) loss. Exposure to acute stressors results in an increase in the incidence of SEC loss. However, little is known about the detachment of SEC from the epithelial sheet. We have used scanning and transmission electron microscopy to study mechanisms of SEC loss from the gastric mucosae of normal, fasted rats and of rats exposed to acute stressors. In fasted control animals SEC loss occurred primarily via extrusion of individual interfoveolar cells and only rarely by degeneration in situ. Each extruding cell was surrounded by a rosette-like configuration of adjacent, encroaching SEC. Mucosal integrity is maintained. Short term exposure to acute stressors results in an increase in the incidence of extrusive cell loss. Continued exposure to stressors also increases the incidence of degeneration in situ of isolated SEC or groups of SEC. Extrusion provides a mechanism for the necessary removal of gastric SEC. Acute stress may override or exhaust the extrusive mode, producing, via ischemia or surface diffusion of cytotoxic agents, SEC degeneration in situ and breaks in the mucosal barrier.
胃黏膜的特点是表面上皮细胞（SEC）丢失率高。暴露于急性应激源会导致SEC丢失发生率增加。然而，关于SEC从上皮层脱离的情况却知之甚少。我们利用扫描电子显微镜和透射电子显微镜研究了正常禁食大鼠以及暴露于急性应激源的大鼠胃黏膜中SEC丢失的机制。在禁食对照动物中，SEC丢失主要通过单个胃小凹间细胞的挤出发生，极少通过原位变性发生。每个挤出的细胞被相邻的、侵入的SEC呈玫瑰花结样包绕。黏膜完整性得以维持。短期暴露于急性应激源会导致挤出性细胞丢失的发生率增加。持续暴露于应激源也会增加孤立的SEC或SEC组原位变性的发生率。挤出为胃SEC的必要清除提供了一种机制。急性应激可能会超越或耗尽挤出模式，通过细胞毒性剂的缺血或表面扩散，导致SEC原位变性和黏膜屏障破裂。
